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Fasciitis
Published in Maher Kurdi, Neuromuscular Pathology Made Easy, 2021
Other associated histological features include prominent eosinophilia, perimysial inflammation, and perifascicular atrophy. Necrotizing granuloma are occasionally seen in the biopsy. The condition should be distinguished from the perimysial inflammation called perimyositis.
Pulmonary hypertension induced by drugs and toxins
Published in Philippe Camus, Edward C Rosenow, Drug-induced and Iatrogenic Respiratory Disease, 2010
Kim Bouillon, Yola Moride, Lucien Abenhaim, Marc Humbert
l-tryptophan is an essential amino-acid that is normally ingested as a constituent of dietary proteins. l-tryptophan supplements are used by some people for disorders such as premenstrual syndrome, insomnia and depression. In October 1989, three patients in New Mexico had a syndrome in which eosinophilia was accompanied by severe myalgias. This syndrome was associated with l-tryptophan ingestion.126 It became a newly recognized disease named eosinophilia–myalgia syndrome (EMS) with the following Centers for Disease Control definition: peripheral blood eosinophilia (> 109/L) and generalized, disabling myalgias without other recognized causes. The apparent median latency period was 127 days.126 EMS is a multisystemic disease; other clinical manifestations include pulmonary involvement (interstitial infiltrates and pleural effusions), skin rash and oedema, axonal polyneuropathy, perimyositis, and possible adverse neurocognitive effects.126 Pulmonary vascular involvement has rarely led to pulmonary hypertension. It has gradually resolved except in a few catastrophic cases. Case–control studies conducted by state health departments confirmed the association of l-tryptophan use with EMS.126 In November 1989, the FDA recalled all l-tryptophan-containing dietary supplements. After that, the number of new cases dropped sharply. In August 1990, over 1500 cases of EMS had been reported in the USA. Epidemiological studies clearly linked illness to the ingestion of tryptophan produced by a single manufacturer in Japan, and the time course of the epidemic was most consistent with it being caused by a product dimeric tryptophan contaminant 1,1’-ethylidenebis [L-tryptophan] known as peak E.126 However, no aetiological agent has been identified. Lung biopsy specimens have been collected among female patients taking L-tryptophan for 1–9 months prior to developing rapidly progressive shortness of breath. They showed both interstitial inflammatory infiltrates with lymphocytes and small numbers of eosinophils, as well as vascular changes with arterial and arteriolar medial hypertrophy being accompanied by mild pulmonary hypertension.127
Rare forms of inflammatory myopathies – part I, generalized forms
Published in Expert Review of Clinical Immunology, 2023
Claudio Galluzzo, Ilaria Chiapparoli, Ada Corrado, Francesco Paolo Cantatore, Carlo Salvarani, Nicolò Pipitone
Eosinophilic myositis (EM) is characterized by a predominant eosinophilic infiltrate of the muscles and often, but not invariably, blood eosinophilia [101,102]. EM be idiopathic, or associated with the hypereosinophilic syndrome (HES), parasite infection, and certain drugs such as methimazole [101,103]. EM is usually classified into three main forms: diffuse EM, focal EM, and eosinophilic perimyositis (EPM) [101,102]. In all forms, subjects in their 40s-50s are particularly affected, with a roughly equal male to female ratio.
Spontaneous resolution of focal eosinophilic myositis of the adductor pollicis complicated by lung lesions
Published in Modern Rheumatology Case Reports, 2020
Sayuri Yamashita, Hidenaga Kawasumi, Makiko Kimura, Mutsuto Tateishi
The present case also had pulmonary lesions. Most FEM patients do not appear to have systemic manifestations [5]; in contrast, patients with eosinophilic polymyositis and eosinophilic perimyositis have systemic symptoms (most commonly fever and gastrointestinal symptoms). To the best of our knowledge, this is the second report of FEM complicated by pulmonary lesions. The first patient had a pleural effusion (patient 10 in Table 2), whereas the present patient had GGO detected on chest CT. FEM complicated by GGO has not been previously reported. In contrast, about half of patients with polymyositis and dermatomyositis exhibit interstitial lung disease (ILD) [14]. Pulmonary lesions in polymyositis and dermatomyositis negatively affect life expectancy, and require management with glucocorticoids or immunosuppressive agents [14]. Idiopathic acute eosinophilic pneumonia, which presents as lung eosinophilia, also requires systemic glucocorticoids [15]. A few cases of mesalazine-induced eosinophilic pneumonia have been previously reported [16–18]. Pulmonary symptoms appeared 1–10 months after initiation of mesalazine treatment, and resolved after discontinuation of mesalazine. In the present case, FEM and GGO also disappeared, despite continuation of mesalazine. While mesalazine-induced eosinophilic pneumonia could be ruled out, an allergy to unknown antigen was suggested. With respect to treatment, myositis in the present patient improved without treatment. We watched the patient without glucocorticoids because no symptoms were found other than the swelling of the left hand at the time when the patient was admitted to our hospital. Myositis in FEM has been reported to resolve spontaneously; however, relapses can occur even years after the initial manifestation [2]. Rapid responses to glucocorticoids have also been reported, and some patients with FEM received NSAIDs. In our literature review (Table 2), 7 of 11 patients received glucocorticoids. In the present case, both myositis and lung lesions improved spontaneously. Further studies are required to determine whether patients with FEM require therapeutic intervention.